Abstract
Long non-coding RNAs (lncRNAs) can regulate gene expression at different levels and are widely participate in various physiological and pathological processes. Emerging evidences suggests that a number of differentially expressed lncRNAs are involved in tumorigenesis. However, the function and expression regulation of a vast majority of these unique RNAs is little known. Here, we found that the lncRNA Ras suppressor protein 1 pseudogene 2 (RSU1P2) is upregulateded in cervical cancer tissues and has a tumour-promoting role. We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. The transcription factor N-myc forms a positive feedback loop with RSU1P2 by in turn activating its expression, thereby enhancing its oncogenic capacity. Hence, cancer-selective targeting of RSU1P2 could have strong benefits.
Highlights
The availability of high-throughput technology offers new opportunities to understand genome function through precise and high resolution mapping of the transcriptional genomic landscape
We revealed that Ras suppressor protein 1 pseudogene 2 (RSU1P2) acts as a competitive endogenous RNA through regulating the expression of IGF1R, N-myc and EphA4
We revealed that the binding of RSU1P2 to the let-7a miRNA relieved the suppression of the let-7a-targeted genes IGF1R, N-myc and EphA4, which may explain role of RSU1P2 in tumorigenesis of cervical cancer
Summary
The availability of high-throughput technology offers new opportunities to understand genome function through precise and high resolution mapping of the transcriptional genomic landscape. A large number of non-protein coding functional transcripts are encoded by the mammalian genome, as reviewed previously [1, 2]. Elegant studies have shown that lncRNAs can regulate gene expression at different levels and widely participate in various physiological processes, including nuclear import, alternative splicing, and epigenetics. These molecules can act as structural components, as regulators of mRNA decay and even as precursors to small RNAs [7]. H19, a 2.3-kb lncRNA, is upregulated in various human cancers, including hepatocellular, bladder and breast carcinomas, suggesting an oncogenic function [9]. The oncogenic lncRNA metastasisassociated lung adenocarcinoma transcript 1 (MALAT1) has been found to act as a decoy for splicing factors leading to splicing malfunctioning [15]
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